부산대학교 도서관

RationaleAntenatal inflammation, usually associated with chorioamnionitis, is a major cause of premature birth. As inflammation could depress respiratory drive, we have examined the effect of clinical chorioamnionitis (CCA) on spontaneous breathing in premature infants at birth.MethodsInfants with CCA born <30 weeks’ gestation were matched with control infants based on gestational age (±6 days), birth weight (±300 g), antenatal corticosteroids, sex and general anaesthesia. The primary outcome was breathing effort, assessed as minute volume (MV) of spontaneous breathing. We also measured tidal volume (Vt), respiratory rate (RR) and apnoea in the first 5 min and additional physiological parameters in the first 10 min after start of respiratory support.ResultsNinety-two infants were included (n=46 CCA infants vs n=46 controls; median (IQR) gestational age 26+4(25+0–27+6) vs 26+6(25+1–28+3) weeks). MV and Vt were significantly lower (MV: 43 (17–93) vs 70 (31–119) mL/kg/min, p=0.043; Vt: 2.6 (1.9–3.6) vs 2.9 (2.2–4.8) mL/kg/breath, p=0.046), whereas RR was similar in CCA infants compared with controls. Incidence of apnoea was higher (5 (2-6) vs 2 (1-4), p=0.002), and total duration of apnoea was longer (90 (21-139) vs 35 (12-98) s, p=0.025) in CCA infants. CCA infants took significantly longer to reach an oxygen saturation >80% (3:37 (2:10–4:29) vs 2:25 (1:06–3:52) min, p=0.016) and had a lower oxygen saturation at 5 min (77 (66–92) vs 91 (68–94) %, p=0.028), despite receiving more oxygen (62 (48-76) vs 54 (43-73) %, p=0.036).ConclusionCCA is associated with reduced breathing effort and oxygenation in premature infants at birth.